Gain-of-function mutations of the genes of KIT proto-oncogene receptor tyrosine kinase (KIT) or the platelet-derived growth factor receptor alpha (PDGFRA) resulted in the constitutive activation of these receptors, thus leading to the induction of GIST (Hirota et al., 1998; Rubin et al., 2001; Heinrich et al., 2003b) and imatinib mesylate (Gleevec), one receptor tyrosine kinase inhibitor, was found to competitively and effectively inhibit KIT and PDGFRA at submicromolar concentrations (Joensuu et al., 2002). This evidence concerns the gene KIT and gastrointestinal stromal tumor.